Midterm 1 - UNIT 04 Flashcards

1
Q
What is a carb?
=
Types of dietary carbs
1
2
3
A

= ‘hydrate of a carbon’ - manufactured by plants

1 Sugars
2 Starch
3 Fibre

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2
Q
1) SUGARS
3 types:
1
ex
2
ex
3
ex
A

1 Monosaccharides: simplest form - 3to9 C atoms (Glucose, Fructose, Galactose)

2 Disaccharides: 2 monosacc - chemically bound
(Lactose, Maltose, Sucrose)

3 Sugar alcohols: manufactured - derived from monosacc - used as sweetener

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3
Q
2) STARCH
=
Animals vs Plants
P: 1
P: 2
A

= storage form of glucose
A: glycogen
P: starch & fibre

1 Amylose: curled - makes up 1/4 of starch in food —LESS bioavailable

2 Amylopectin: straight chain- makes up 3/4 starch in food - branch - MORE bioavailable
2 Amylopectin

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4
Q
3) FIBRE
=
2 types:
1
function:
ex
2
A

= Non-digestible carbs (in plants)
- complex carb

1 Soluble fibre

  • dissolves in hot water - forms a gel
  • SLOWS gastric motility
  • FULLER feeling
  • absorbs FA (lymph doesn’t)
  • decreases Cholesterol/CV disease
  • ex: oat, bran, dried beans
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5
Q

2
function:
ex

A

2 Insoluble Fibre
= doesn’t dissolve in hot water
- absorbs water into GI system
- speeds up intestinal motility / decreases absorption time
- decreases chance of type 2 DM
- too much insoluble –> nutr deficiencies
- ex: fruit skins, veggies

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6
Q

Path of consumed carbs through the body:

4 steps

A

1 Starts @ mouth - amylase from salivary glands

2 monosaccharides = end product of carb digestion –> enter capillaries of intestinal villi

3 Monosacc travel to liver VIA hepatic portal vein

4 In liver, galactose and fructose are converted to glucose then glucose to storage (most not all)

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7
Q

WHY do we need carbs?
(1-3)
1
fuel source for ____

2

3

A

1 Energy Needs
for neurons (ONLY uses glucose) - can used ketones
- RBCs only use glucose
- need carbs to metabolize other fuels

2 Pregnancy
- placenta and fetus only feed off glucose

3 Spares muscle protein degradation for energy

  • glucose must be synthesized from muscle protein (if body doesn’t have enough carbs - liver will break down muscle)
  • AA converted to 1 ketone bodies 2 FA 3 glucose (if muscle protein is broken down)
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8
Q

CARBS & Energy

  • we store glucose as what in where
  • what has higher conc
  • which has higher total energy
A
  • as glycogen in liver and skeletal muscle cells
  • LIVER has higher conc
  • MUSCLE has higher overall energy as there is more space - more muscle
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9
Q

Physiological pathway of glucose molecules after a meal is consumed
1-7
(1-3)

A

1 when person eats - blood gluc rises
Carbs go thru mechanical and chem digestion to intestines and absorbed into bloodstream and circulated

2 high blood glucose gets stimulates — pancreas to release INSULIN in the blood—
[endocrine organ - produces insulin and glucagon and hormones enter blood to perform their function]

  • Insulin detects extra glucose molecules - when insulin is in the blood it will go to target cells (liver and muscle) to trigger them to uptake glucose for storage

3 Insulin stimulates the uptake and storage as glycogen and stimulates the conversion of excess glucose into fat for storage

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10
Q

(4-7)

A

4 as the body uses glucose - levels decline in the blood- pancreas will detect the drop

5 low blood glucose stimulates pancreas release of glucagon –> blood
[specifically targets the LIVER not muscle]

6 Glucagon stimulates the liver to breakdown stored glycogen and release glucose into the bloo

7 blood glucose beings to rise to restore healthy levels (not to after meal levels)

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11
Q
GLYCEMIC INDEX
= 
2 standards:
factors affecting GI of foods:
1 =
ex
2
- concern with consuming high GI foods...
3
ex
A

= a measure (no units) of the potential of food to raise blood glucose levels
- how quickly blood glucose rises after a meal

: 1 slice of white bread or pure glucose

1 Proportion of carb content of ingested food
[more carb higher GI]
ex - ice cream = 61 GI
boiled potato = 85 GI

2 Type of carb
simple (sugar)
- increases GI
complex starch
- decreases GI as it stays in GI tract longer

… plays an indirect role with fat storage - insulin promotes glucose from blood–> storage - fat promotion effect

3 Cooking
- heat helps to disrupt chemical bonds
- faster digestion
pasta boiled 5 min = 34
          boiled 10 min = 40
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12
Q

GLYCEMIC LOAD
= (eqn)

ex

A

= GI x amount of available carbs in food source / 100

  • how HIGH blood glucose gets
  • predictor of developing type 2 DM & CV disease

ex: corn muffin
GI = 102 carbs = 29 g = GL 30

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13
Q

Process of GLUT 1 and GLUT 4

embedded :

what happens when many glucose molecules appear…

A

= glucose transporter
: in the muscle fibre membrane to move glucose into muscle cytoplasm

  • glucose moves through the blood, enters extra-cellular space - will bind to asparagine 45 - form a chemical bond THEN GLUT-1 transporter moves glucose into cytoplasm to store or use as fuel
    WHEN MANY GLUC APPEAR…
    this exceeds capacity of GLUT-1 therefore insulin will bind to specific protein receptor in muscle fibre mem to ACTIVATE enzymes of interior muscle fibre - GLUT-4 = same as GLUT-1 but insulin calls upon it
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14
Q
Pancreatic Hormones
1
produced by:
function:
overall effect:
2
produced by:
function:
- stimulates \_\_\_\_\_\_ =
overall effect:
A

1 INSULIN
: beta cells of pancreas
: helps take in glucose from blood - target cells — stimulates liver and muscle to store as glycogen
: lowering blood glucose

2 GLUCAGON
: alpha cells of pancreas
: signals starved state - very low glucose levels— stimulates breakdown of glycogen from liver –> blood
- Gluconeogenesis = production of glucose from AA
: raises blood glucose levels

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15
Q
CARB - related disorders
1 Diabetes Mellitus
=
characterized by:
results from:

Diabetes insipidus:

A

= a disorder of carb metabolism characterized by hyperglycemia & glycosuria - results from inadequate production or utilization of insulin

  • more people affect by type 2

: impaired water re-absorption in kidney (lack of ADH or vasopressin)

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16
Q
TYPE 1
=
No \_\_\_\_\_ cells =
1
2
3
consequences:
 - additionally-

risk factors:

A

= auto-immune disorder
- beta cells are ingested by immune system

No beta cells=
1 no insulin production
2 leads to hyperglycemia 
3 no uptake of glucose into target cells
\: muscle - no activation of GLUT-4
\: liver - no activation of GLUT-2
 - liver 'sees' no glucose brought in and therefore thinks 'low blood glucose' 
THEN liver increases glyconeolysis which makes hyperglycemia worse

: genetics & family history

17
Q

TYPE 1 CONT
Energy utilization:
what becomes fuel source

A

: b/c glucose is not able to reach cell storage - body says ‘starvation state’ THEn fuel source becomes:

(A) FA - no insulin = no 7TM receptor binding = no inhibition of triglycideride lipase
- many stored FA are broken down

(B) Muscle protein eventually

18
Q

Renal Threshold:

- urinary glucose attracts…

A

: blood glucose level in which glucose is not re absorbed from the the kidneys (glycosuria)
- exceeds capacity of renal tubules for reabsorption

… water molecules = consistent thirst and frequent urination - TYPE 1 symptom

19
Q
Complications:
Insulin Deficiency
1
2
3
4
A

1 increased adrenalines , increasing metabolism (catechloamine) increasing muscle degradation (cortisol) and increasing glucose in blood (glucagon)

2 leads to increase lipolysis

3 increase production of ketoacids (decrease body pH)

4 (3) leads to (4) reflexive increase in respiration (Kussmaul respirations - form of hyperventilation)

20
Q

Overall complications:
1-4

acute complication:

A

1 increase blood pressure due to increased blood glucose molecules
2 kidney disease - excessive pressure and filtration
3 peripheral vascular disease
4 blindness - related to reductions in capillary-fed blood flow

: diabetic ketoacidosis

21
Q

MANAGEMENT
_____ supply
factors:

A

exogenous insulin supply

: activity, eating pattern, timing of latter 2 and injection

22
Q

TYPE 2 DM

diagnosis:
WHY:

insulin activates GLUT-4 but so does-
management:
risk factors:

A

= non-insulin dependent (was adult onset but this is no longer true)
- related to increase obesity rate of children

: same as type 1 & chronically high levels of blood glucose under fasting conditions

: insulin supply is initially OK — glucose using cells (liver and muscle) are ‘insulin resistant’

  • muscle contraction - makes exercise effective management

: eating pattern - decrease simple carbs// physical activity
: family history/ genetics/ overweight, low HDL or high TG/ gestational diabetes

23
Q
Syndrome X (metabolic syndrome)
- ppl most likely in pre-diabetes stage
Gestational Diabetes:
cause:
risk factors:
complications:
management:
A

: development of DM as result of pregnancy
C: increase insulin resistance— progesterone inhibitory effect of beta cells — human placental lactogen (hormone) stimulates lipolysis - implicated in insulin resistance
R: existing DM, family history, overweight, age, ethnic group
C: high blood pressure, lg birthweight
jaundice and brain/growth development
M: dietary— monitoring — post birth monitor